Type II spiral ganglion afferent neurons drive medial olivocochlear reflex suppression of the cochlear amplifier
Kristina E. Froud,
Ann Chi Yan Wong,
Jennie M. E. Cederholm,
Matthias Klugmann,
Shaun L. Sandow,
Jean-Pierre Julien,
Allen F. Ryan and
Gary D. Housley ()
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Kristina E. Froud: School of Medical Sciences, UNSW Australia
Ann Chi Yan Wong: School of Medical Sciences, UNSW Australia
Jennie M. E. Cederholm: School of Medical Sciences, UNSW Australia
Matthias Klugmann: School of Medical Sciences, UNSW Australia
Shaun L. Sandow: School of Medical Sciences, UNSW Australia
Jean-Pierre Julien: Laval University, Institut Universitaire en santé mentale de Québec
Allen F. Ryan: University of California San Diego, and Veterans Administration Medical Center
Gary D. Housley: School of Medical Sciences, UNSW Australia
Nature Communications, 2015, vol. 6, issue 1, 1-9
Abstract:
Abstract The dynamic adjustment of hearing sensitivity and frequency selectivity is mediated by the medial olivocochlear efferent reflex, which suppresses the gain of the ‘cochlear amplifier’ in each ear. Such efferent feedback is important for promoting discrimination of sounds in background noise, sound localization and protecting the cochleae from acoustic overstimulation. However, the sensory driver for the olivocochlear reflex is unknown. Here, we resolve this longstanding question using a mouse model null for the gene encoding the type III intermediate filament peripherin (Prph). Prph(−/−) mice lacked type II spiral ganglion neuron innervation of the outer hair cells, whereas innervation of the inner hair cells by type I spiral ganglion neurons was normal. Compared with Prph(+/+) controls, both contralateral and ipsilateral olivocochlear efferent-mediated suppression of the cochlear amplifier were absent in Prph(−/−) mice, demonstrating that outer hair cells and their type II afferents constitute the sensory drive for the olivocochlear efferent reflex.
Date: 2015
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms8115
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DOI: 10.1038/ncomms8115
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